peptic ulcer disease - department of surgery, cuhk ulcer-dr... · prepyloric ulcer 4.high lesser...
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+Peptic ulcer disease
Dr Anthony Yuen Bun TeohDeputy Director of EndoscopyHonorary Clinical Assistant ProfessorAssociate ConsultantDivision of UGI Surgery
+Peptic ulcer
Definition
Breach in the mucosa of the GIT as a result of the action of gastrin on parietal cells leading to production of acid
Types
Duodenal ulcer
Gastric ulcer
Small bowel ulcer e.g. meckel’s diverticulum
+Classification – John’s criteria
Types
1. Lesser curve (body) ulcer
2. Duodenal ulcer + 1esser curve ulcer
3. Prepyloric ulcer
4. High lesser curve
Most common location: along the lesser curvature of the stomach !!
+Causative factors
Most common causes
Helicobacter pyloriWHO Class I carcinogen
NSAIDS
Other factors
Stress
Smoking
Caffeine
Infection: CMV/HSV
HyperPTH
Chronic liver disease
Chronic renal disease
Zollinger Ellison disease
+H. Pylori
Gram-ve spiral shaped microaerophilic bacterium
Colonises gastric epithelium
Direct contact
+Pathogensis
Not all patients with H. Pylori infection develop ulcers
Bacterial factorsMany different strains of H. PyloriVirulence differentSome cause gastritis and others ulcer
Host factorsH. Pylori binds preferentially to Lewis antigen (part of complex determing blood group)
infection in blood gp O
+Mechanism of injury [1]
1. Local epithelial damage
Secretion of cytotoxins, urease, vacuolating cytotoxin, heat shock proteinsDamages mucosal layer and allows action of acid on epithelial cellsLeads to local inflammation exacerbating mucosal insults
+Mechanism of injury [2]
2. Increase gastric acid production
Local inflammation inhibits secretion
Increased gastrin and pepsinogen release
Increase acid within duodenum => gastric metaplasia in duodenum => colonization in duodenum => inflammation and DU
+H Pylori Class I carcinogen
+Methods of Dx [1]
Gold standard
Endoscopic bx + histological examination
Rapid urease test
Test for urease activity
pH of medium
+Methods of Dx [2]
Urease breath testMeasurement of 13CO2 / 12CO2 ratio in baseline and post-ingestion samples
Serology (IgG) –antibody testing-
not useful for post treatment success
Stool antigen detection
+Treatment – American college of gastroenterology guidelines
+Treatment of Uncomplicated ulcers
Correct etiological agentsEradication of H. pyloriAvoid NSAID and aspirin, or use protective agents with aspirin, or use COX-2 inhibitorTreat underlying conditions
Ulcer healing drugsPPI 4-6/52
Fu endoscopyGU – risk of malignancy
+Population-based estimates from US Nationwide Inpatients
Bashinskaya et al. J Glob Infect Dis 2012
BDUPDU
Vagotomy
HSV
Gastrectomy
Elective ulcer surgery almost extinct!!
+Ulcer complications
HaemorrhageMost common among all ulcer complications~10% of peptic ulcers present with bleeding
PerforationRapidly decreasing trendMean age of presentation becomes older, ?NSAID use
ObstructionUncommon
Penetration
+What to do for ulcer complications
As a surgeon…we want …
Control
Short term (Immediate, life saving)
Long term (Late, mainly to prevent recurrence)
+Peptic ulcer bleeding
PresentationBlood in the form of
Tarry stoolCoffee ground vomitingHaematemesis
AnaemiaExertional dyspneaMalasie
PR: melaenaHypovolaemic shock
+3 Essential Elements in the Management of GIB 3 Essential Elements in the Management of GIB –– SShort term controlhort term control
Resuscitation– Crystalloid (First choice)– Plasma expander – Blood (in desperate situations)
Localisation– Endoscopy– Other Imagings
Haemostasis– Endoscopic intervention (First line)– Surgery
+Resuscitation….. A, B, C
Large bore IV cannula and fluid/Blood
Closer monitoring of BP, pulse, SaO2
+/- Central venous pressure
Urine output (Hourly) – Foley cath
+Hypovolumic shock signs
Blood loss (ml) <750 750-1500 1500-2000 >2000
Blood loss (%) <15 15-30 30-40 >40
Pulse rate <100 >100 >120 >140
Blood pressure Normal Normal Decreased Decreased
Pulse pressure Normal or increased Decreased Decreased Decreased
Respiratory rate 14-20 20-30 30-40 >35
Urine output (ml) >30 20-30 5-15 Negligible
Mental status Slightly anxious Mildly anxious Anxious and
confused
Confused and
lethargic
Fluid replacement Crystalloid Crystalloid Crystalloid and
blood
Crystalloid and
blood
+Glasgow Blatchford bleeding score Admission risk markers Score
valueAdmission risk markers Score value
Blood urea (mmol/L) Systolic blood pressure
6.5-7.9 2 100-109 1
8.0-9.9 3 90-99 2
10.0-24.9 4 <90 3
≥25 6 Other markers
Hemoglobin for men (g/L) Pulse ≥ 100/min 1
120-129 1 Presentation with melaena 1
100-119 3 Presentation with syncope 2
<100 6 Hepatic disease 2
Hemoglobin for women (g/L) Cardiac failure 2
100-119 1
<100 6
+GBS score
One of many scoring systems (CUHK scores Rockhall score)
Calculated based on admission criteria
Accurately predicts need of intervention and death
Score >8 = 41% mortality and a rebleeding rate of 42.1%.
high risk patientsadmitted to HDU
Consider urgent endoscopy
+
PPI infusion before endoscopy
Less patients with bleeding ulcers
Less endoscopic therapy
More clean based ulcers
+Need of Urgent Endoscopy?
Most (90%) bleeding stopped spontaneously
Urgent OGD is indicated when there are signs of ongoing bleeding:
Fresh Haematemesis
Unstable Haemodynamics despite resuscitation
Repeated fresh melaena and drop in Hb
+Role of Endoscopy
Identify the source of bleeding
Assess risk of re-bleeding
Endoscopic hemostasis
Forrest’s Classification of SRH
Ia
IIa IIb IIc
Ib
+SRH: Significance?
+Haemostasis
EndoscopicInjection therapyCoaptive coagulation (Thermocoagulation)Laser coagulationMechanical devices
e.g. clips
Surgery
+Injection Therapy
Agents used
Adrenaline solutionlocal tamponadevasoconstrictionplatelet aggregation
SclerosantsPolidocanols, absolute alcohol, or STD
Saline
+Coaptive coagulation
Direct pressure + heat energy
heat probe
bipolar probe
+Laser Coagulation
Nd: YAG laser
Non-contact thermal method
Laser energy transferred to heat when interacts with tissue around the bleeding vessel
Less preferred
+Mechanical Devices
Haemoclips
+Efficacy & risk of rebleeding
All achieve initial haemostasis > 90%
Rebleeding occurs in 15%-20%
Patients prone to rebleeding if:Shock on admission
SRH: Forrest Ia>Ib>IIa>IIb
Large ulcer
? How to secure haemostasis
+To enhance haemostasis
Combined therapyAdrenaline injection + Heater probe
Reduce gastric acidityTo stablise the coagulumIntravenous high dose PPI
Eradication of HP during acute stage: no role
+Proton pump inhibitors
PPI infusion reduces rate of recurrent bleeding but not mortality
+After successful endoscopic haemostasis
Close monitoring
Transfuse if indicated
Acid suppression therapy
? Early refeeding
Highest risk of rebleeding: first 72 hours (~94%)
HP eradication for infected patients when discharged
Surgery is indicated only if:Surgery is indicated only if:
Failed primary endoscopic haemostasis
Rebleeding in-hospital– After repeated endoscopic treatment
Ongoing transfusion > defined value, eg, 8 units
+Surgical Options For Bleeding DU
SmallPlication (Suture) of bleeding vesselExclusion of ulcer (Pull surrounding mucosa to cover the ulcer)
Large Distal partial gastrectomy
+Bleeding GU
Distal ulcerDistal gastrectomy
Proximal ulcerUlcer excision + acid reduction procedure
Unstable patientUlcer excision alone
The goalThe goal
To stop bleeding (To save life)To rescue with minimal morbidity and mortality
+/- To control ulcer diathesisLengthy definitive acid reduction surgery may not be necessary
Perforated Peptic Ulcer
Sudden epigastric pain
Rapidly generalised
Board-like rigidity
First 4-6 hrs:Chemical peritonitis
> 6 hours: Bacterial peritonitis
CXR: free gas under diaphragm
(50%-70%)
+PPU
Prognosis worse if:Delay presentation (>24 hours)
Old age
Hypotension
Associated medical illness
Boey et al, BJS 1985
APACHE II score (less practical)Lee et al, BJS 2001
+PPU
DU: 80-90%Mostly related to Helicobacter pylori
GU: 10-20%More related to NSAID useHalf also got H. pylori infection
+Perforated peptic ulcers
• Remains a common surgical emergency in some places like Hong Kong and China
• Annual number of new cases in HK Mortality• 2008 447 12.3%
• 2009 492 11%
• 2010 494 8.5%
• Acute management
Immediate resuscitation
Antibiotics
Timely surgery to seal the perforation and cleanse the peritoneal cavity
+Management of PPU
ResuscitationFluid replacment, correct electrolytes
Nasogastric tube
IV antibiotics
IV acid suppression
Close monitoring
Conservative vs treatment operativeCrofts NEJM 1989
Surgical treatment of PPUTwo components1. Graham’ Patch repair (≤ 2cm in size)
2. Peritoneal lavage
> 6L of normal saline
Antiseptic solution no longer used
+Patch repair of PPU
Conventionally done by open surgeryRequire a laparotomy woundHigh chance of wound infectionPostop wound painDelay recovery
+Patch Repair of PPU
Now can be performed under laparoscopySafe with ulcer less than 1 cm in diameter
Leakage rate less than 5%
Less postop wound pain
Less analgesic requirement
+% patients receiving lap patch repair in PWH
+Role of open surgery in the current era
Patients at high risk of mortality and morbidity
ASA scoreBoey scoreLarge ulcersNeed of inotropes
Teoh et al 2013
+Types of open surgery
2 principles
1. Control of perforationPDU
<2cm patch repair + peritoneal lavage
>2cm partial gastrectomy + closure of duodenal stump
Vagotomy + pyloroplasty may be difficult due to scarring
PGU
Benign vs malignant
Ulcer bx + patch repair + acid control
Excision of ulcer + acid control
Gastrectomy
+What about the long term outcome?
Before 90’s
Definitive operations such as highly selective vagotomy or gastrectomy were advocated by most surgeons as the treatment of choice for PPU
Because long term FU of simple patch repair is associated with high risk of ulcer relapse
Estimated recurrent ulcer rate at one year: 40%
+RCT of Hp eradication in PPU
2
16
38
22
05
10152025303540
Quadruple Omeprazole
Nu
mbe
r of
pat
ien
ts
Ulcer recurred
Ulcer not recurred
**
ψ P < 0.001
*
Ng et al, Ann Surg 1999
+Meta-analysis
+Is there need to control ulcer diathesis?
Control ulcer diathesis (pre PPI years)TV + drainage procedure
HSV
life-long PPI and HP eradicated, risk of rebleeding is low
+Summary
For PPULife saving First
Simple repair whenever possibleThorough peritoneal toileting
Control ulcer diathesisEradication of H. pyloriWithdraw NSAID if possibleDefinitive surgery only if giant perforation not amenable to repair
+Zollinger Ellison’s disease
Gastrinoma
Gastrinoma triangle: CBD & CHD junction, D2/3 junction, neck & body of pancreas
2/3 multifocal in pancreas
2/3 malignant
Dx: fasting serum gastrin levels, (false +ve: causes of achlorydria), secretin provocation test
+Treatment
Control acid: PPI
SurgeryLocalisation
CT, EUS, somatostatin receptor scintigraphy (SRS) – 80% sensitivity, can detect distant mets
Failure to localize: Controversial to explore
Excision
Endoscopic
Surgery
+Gastric outlet obstruction
Long history of peptic ulcer / dyspepsia
Wax and wane
Change of periodicity
Repeated vomitingUndigested, non-bile-stained food
Dehydration and weight loss
+Gastric outlet obstruction
Metabolic disturbanceDehydrationHypokalaemiaHypochloriaemiaMetabolic alkalosisParadoxical aciduria
+Initial management
DecompressionNPONG tube
RehydrationIsotonic crystalloidK replacementNo need to adjust the alkalosis
Further investigationNeed to rule out malignancy!
+Investigation
Water soluble contrast meal
Don’t perform Barium study
Endoscopy +/- biopsy to exclude malignancy
CT Abdomen + pelvis with contrast
+Treatment [1]
EndoscopicBalloon dilatationLong-term result not satisfactory, with half of the patients developing recurrenceReserved for poor risk patients
+Treatment [2]
SurgicalDrainage of the stomach into small bowelAbolish the ulcer diathesis -vagotomyCan be done under laparoscope
+Ulcer penetration
+
+Conclusion
Peptic ulcer disease is an endemic disease in HK
Associated with potentially life threatening complications
Prompt treatment is necessary to improve outcomes
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